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. 2021 Aug 2;15:657884. doi: 10.3389/fnsys.2021.657884

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Copyright © 2021 Li, Dong, Li, Zhang, Bing, Chu, Cui and Qiu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Blockade of GluN2A abolished the chronic ethanol exposure-induced enhancement of facial stimulation-evoked MF–GC synaptic transmission. (A) Representative field potential traces showing that the air-puff stimuli (10 ms, 60 psi; 5 pulse, 20 Hz) on the ipsilateral whisker pad evoked field potential responses, recorded from the GL of control (upper) and ethanol-exposed mice in treatments of ACSF, PEAQX (10 μM), and recovery (washout). (B) Summary of data showing the absolute (±SEM) amplitudes of N1–N5 in treatments with ACSF, PEAQX, and recovery (washout) in control mice. (C) Summary of data showing the absolute amplitudes of N1–N5 in treatments with ACSF, PEAQX, and recovery (washout) in ethanol-exposed mice. (D) Bar graph showing the mean amplitude of peaks recorded in the presence of ACSF in control and ethanol-exposed mice. (E) A bar graph showing the mean amplitude of peaks recorded in the presence of PEAQX in control and ethanol-exposed mice. (F) A bar graph with individual data (Symbols of different colors) showing the normalized amplitude of N2 in each treatment. (G) A bar graph with individual data (Symbols of different colors) showing the normalized AUC of N2 in treatments with ACSF, PEAQX, and recovery (washout). n = 8 in each group. *P < 0.05 vs. ACSF; #P < 0.05 vs. control.